Iah writes:
Hi folks!
I’ah (pronounced: eye-ah) here! I must say I really enjoyed you all struggling with the pronunciation of my name. I realised my error in not providing a pronunciation note after I sent the email. I am female by the way. And to Kathy, I did order the paperback form of Spillover. Excellent so far.
Thank you for your responses to my question – I found it very helpful. Keep up the good work – I’m recommending you to all my virology friends!
Kindest regards,
I’ah
Tolga writes:
Is there any lab in New York area with a 2 or 3 photon microscope that is willing to do a 3rd party research consulting project? I would appreciate your help.
Thank you
Tolga
Felic writes:
Dear TWiV hosts,
A news regarding the recent Zika outbreak in Singapore triggered my curiosity and I would like to ask your opinions on this matter. News report from a press conference earlier today mentioned that based on the sequencing analysis : “…..the virus belongs to the Asian lineage and likely evolved from the strain that was already circulating in Southeast Asia“. The newspaper article also mentioned that the viruses wasn’t imported from South America.
My questions are as follows:
(1) Does the virus that causes the outbreaks in the Americas differ significantly enough that enable us to differentiate clearly between the the ‘American’ and Asian lineage? I’ve read before that the Zika outbreak in the Americas is caused by the Asian lineage and I’m confused with the statement. Perhaps it’s just a matter of wording and I’m looking forward to details from the research team.
(2) If the Zika outbreak in Singapore comes from an (older) Asian lineage, why the sudden spike? Can it be that there have been multiple Zika infections in the island which remained undetected or perhaps those cases were misdiagnosed as Dengue? Are you aware of any recent studies that try to figure out how prevalent the circulation of Zika in Asia/Africa before the recent outbreaks? Dengue is a common scourge in South East Asia and I won’t be surprised that many previous Zika infections were misdiagnosed as Dengue.
I apologize if these issues have been discussed in previous episodes. I have enjoyed listening to TWIV (and other podcasts in the series) during my daily commute in the past 2 years. The podcasts in the series have reinvigorated my interest in the infectious diseases field, I wish I’ve started listening while I was in college few years ago! Oddly enough, I took Vincent’s virology course in Coursera 3 years ago without listening to any of these podcasts.
Thank you for your excellent contribution to these science outreach avenues. Keep up the good work!
Best,
Andrew B
Jakarta, Indonesia
P.S.
A google search indicates that it’s currently 27 degree Celsius with 79% humidity(!)
Link for the news article:
Robert writes:
I’m reading this book by Donald G. McNeil Jr. (Norton, 2016.) The author is a reporter with the NY Times and very knowledgeable, judging by what I see in the book compared to the discussion of Zika on TWIV.
On p. 86 the author cites a conversation with Dr. Ian Lipkin, who makes a chilling prediction about the future development of apparently healthy babies of mothers with Zika:
“I wouldn’t be surprised if we saw big upswings in ADHD, in autism, in epilepsy, and in schizophrenia.”
Yikes!
Always enjoy your show.
Bob
Phil writes:
Hello Team TWIV,
I was hoping to get the TWIVsight (TWIV insight) or just general thoughts on the attached picture. For those that can’t see the picture, this is an OFF insect repellent stand in a King Soopers grocery store with the advertisement “Protect against the mosquitoes that may carry the ZIKA VIRUS”. I thought this was interesting advertising, not in the least because this is in Denver, Colorado, where Aedes does not live, at least according to the Colorado Department of Public Health and Environment (https://www.colorado.gov/pacific/cdphe/news/zika-travel-warning). I wonder if someone will see this and assume mosquitoes in Colorado can infect them with Zika.
Any thoughts on advertising like this? My friends are divided, some think this is fine since OFF would indeed protect against Aedes, others think this is profiting off fearmongering since we don’t have the relevant mosquito here.
As for the weather, it is currently 60°F (~16 C°) with 65% humidity and light wind in Denver. Thank you all for TWIV, I started listening to TWIV in January and now it is a weekly ritual. It is a great way to keep informed before starting graduate school in a few months.
Cheers,
Phil
Paul writes:
To the twivle seat:
A climate controlled 22C and zero humidity at 25000 feet above the Ohio Valley, reading about the WHO recommendation to delay pregnancy.
The question that comes to my mind is this:
How far is Zika virus itself from being its own vaccine for populations at significant risk?
Isn’t it the case that
….80% of infections are entirely asymptomatic
….The vast majority of symptomatic infections have no serious complications in healthy people that are not pregnant
…the remaining risk from deliberate infection for non-pregnant individuals in affected areas is negligible anyway since everyone expects that virtually everyone in those areas will be exposed to the virus in the coming years anyway
…post infection immunity seems to protect against birth defects associated with subsequent infections?
So, for a family that wants to have children, wouldn’t deliberate infection, coupled with a brief delay in pregnancy until the virus clears be a coherent strategy in the absence of a vaccine?
How much better than the virus itself would a vaccine have to perform to be approved for use in people at significant risk from an accidental infection demonstrated not to be pregnant and on reliable birth control?
While a vaccine for universal use would require a lot more science, the risks associated with deliberate infection do not seem large compared to the risks reality incurred by people seeking to have children?
Steve writes:
Hi Vincent,
Sorry to read of your disappointment on Obama putting off decisions on funding for Zika.
This call from the UK’s MRC came out today, for setting up networks to find new ways to deal with the rise in vector borne diseases. Although the lead for each network looks to have to be in the UK, it seems to me that international research collaborations already seem to be the norm, so, perhaps you and your various colleagues in the TWix disciplines might be able to work up networks to benefit from this new funding stream.
Apologies if I’ve got the whole process mixed up, as I have no experience of any kind of funding, but as much of what the call out mentions is regularly covered in your podcasts, I thought I’d pass it on.
All the best,
Steve
Luton
England
Marion writes:
I have heard you’all discuss antibody-dependent enhancement of infection (ADE) of Dengue several times as a mysterious phenomenon. According to a talk I just heard, one hypothesis to explain ADE may be that it is related to the high proportion of immature Dengue particles in infections. This hypothesis was not the point of the talk I heard: it was mentioned in passing. The hypothesis is that anti-PrM, not anti-E antibodies, are responsible for ADE.
Like many enveloped viruses, Dengue undergoes a final maturation cleavage of the E (Envelope) protein by host furin proteases in the trans-golgi network. In Dengue, this is an inefficient cleavage. The immature protein, found on immature virus particles, is called PrM. Therefore infectious virus is actually a heterogeneous mixture of mature and immature particles. The resulting immune response is also heterogeneous against E and PrM. Apparently, some anti-PrM antibodies may enhance infection; perhaps by maturing the immature particles or facilitating uptake. Apparently they would be cross-serotype reactive. Therefore, residual anti-PrM antibodies from one infection linger and, rather than protecting, enhance subsequent infections. Additionally, each serotype differs in its extent of immaturity. Dengue 4 has more efficient cleavage than Dengue 2, ie, Dengue 2 is the most heterogeneous. I have appended one reference I found on the subject. The speaker mentioned that Dengue patients with disease have more anti-PrM antibodies.
This also explains why a Dengue vaccine is possible, despite ADE, as long as the vaccine presents only E and not PrM as antigen.
The new work on the Cryo-EM structure of Zika show homogeneity, ie, a lack of partial immaturity. Therefore the phenomenon of heterogeneous maturation, at least as a major feature, appears, thus far, to be unique to Dengue. This suggests that Zika would not be expected to display ADE and that ADE would not prevent a Zika vaccine. One caveat I would add is that the virus that was used for EM was produced from furin-over-expressing cells, so the natural situation may differ from this.
BMC Microbiol. 2013 Aug 29;13:194. doi: 10.1186/1471-2180-13-194.
Cristina writes:
Hello,
I am writing to you from Newsy in Columbia, MO, where we have an exclusive three part series on the Zika virus titled “Zika’s Untold War” that might be of interest to you to share.
Landing Page: http://www.newsy.com/social/zika/
In this series, Newsy investigates the roles of the church and government in Salvadoran reproductive rights, the link between Zika and birth defects, the rise of Guillain-Barre syndrome, and recent medical breakthroughs that all highlight the international significance of El Salvador’s struggle to combat the virus.
Trailer: https://www.youtube.com/watch?v=hBWBACyOJxQ
With the 2016 Olympics almost here, the Zika virus continues to make headlines. But Zika is more than just a virus — there’s a story you haven’t heard. El Salvador has seen thousands of suspected Zika cases among its population of just 6 million people. And many more likely go unreported.
Part 1- Zika’s Untold War: Power Vs. The People
https://www.youtube.com/watch?v=Co2DoU6Ldz0
Part 2- Zika’s Untold War: Chain Reaction
https://www.youtube.com/watch?v=qxtNtOUa_G0
Part 3- Zika’s Untold War: The Fight Continues
https://www.youtube.com/watch?v=A8s10EZfNdA
With your help we can bring an awareness to the Zika virus by simply sharing and posting the series to your social media sites and website. Please let me know if you are interested and feel free to use the assets in this email as well as the attached images.
Thank you,
Cristina Carlos
Content Marketing Specialist
Newsy
Dennis writes:
Question about Zika virus host range evolution enabling possible avian reservoirs. (edited)
I’m trying to understand why birds, that are being challenged over and over again with Zika virus via mosquitos bites just like people, do not support the evolution/selection of virus and thus become viremic enough to allow for avian reservoirs of the virus to be created. The birds could be completely asymptomatic.
The Flavivirus can mutate with high frequency especially at certain highly variable genomic locations. Changes at these sites (via low fidelity replication), could alter their coat protein sequence in minor ways. This would include changes that disrupt the binding or enhance to the binding to various important cellular viral receptors. Such changes in the avidity for the various mammalian/avian cellular receptors would be selected if virus replication rates were enhanced in that host. If that were to happen, it would give them the ability to adapt to various hosts and increase their host range. There are four strains of Dengue that likely evolved via such a mutation/selection mechanism. Did these strains receive host range changes as well? How much do we know about the avidity of the Zika, Dengue and WNV for important virus receptors, be they avian or primate? Do we have data about any evolutionary changes among the current Zika virus and thus its current host range?